Clinical & Experimental Cardiology
Open Access

Abstract

Left Atrial Enlargement Correlates with Inflammation and Oxidative Stress in Patients at High Risk for Atrial Fibrillation

Heather L. Bloom, Irfan Shukrullah, William Jang, Richard N. Vest III and Samuel C. Dudley

Objective: To examine the relationship between enlarged left atrial volume and increased blood markers of oxidative stress in patients at high risk for atrial fibrillation.

Design: This is a retrospective study where a single blood draw was taken from a cohort of patients with internal cardioverter-defibrillators, cardiomyopathy and ejection fraction (EF) = 30%, and sent for markers of oxidative stress and inflammation. Left atrial size was obtained from echocardiography.

Setting: Single center, multi-hospital, cohort of 191 patients who underwent subgroup analysis; these patients are a subgroup of those enrolled in a larger, prospective trial, multicenter trial.

Patients: See above

Interventions: Single blood draw, retrospective database/chart review

Outcome Measures: Levels of hsCRP, IL-6, TNF-α, nitrotyrosine, reduced to oxidized cysteine ratio, reduced to oxidized glutathione ratio, derivatives of reactive oxygen metabolites (DROMS) Results: Under univariate analysis, BMI (ρ= 0.003, r= 0.211), IL-6 (ρ=0.03, r= 0.192) and cysteine ratio (ρ=0.004, r=0.242) all correlated with LA enlargement. Binary logistic regression demonstrated that the single factor that best classified normal vs. enlarged LA is cysteine (ρ=.001). The binary logistic model itself is significantly predictive, as indicated by an omnibus test of model coefficients (ρ<.001). When analyzed as a continuous variable, rather than using a cut point, increasing IL-6 levels correlated to increasing LA diameter.

Conclusions: These data suggest an association between IL-6, cysteine and left atrial enlargement (LAE). As LAE is associated with atrial fibrillation, reductions in inflammation and oxidative stress may lead to decreased risk of atrial fibrillation. Treatments to reduce oxidative stress may have potential to prevent development of atrial fibrillation.